Cardiac assist systems aid patients with chronically and unacceptably low cardiac output who cannot have their cardiac output raised to acceptable levels by traditional treatments, such as drug therapy. One particular type of cardiac assist system currently used is a cardiomyoplasty.
Essentially a cardiomyoplasty provides a muscle-powered cardiac assist system. As seen in U.S. Pat. No. 4,813,952 of Khalafalla, incorporated herein by reference, the cardiomyoplasty is a cardiac assist system powered by a surgically-modified muscle tissue, such as the latissimus dorsi. In particular, the latissimus dorsi is wrapped around the heart. An implantable pulse generator is provided. The implantable pulse generator senses contractions of the heart via one or more sensing leads and stimulates the appropriate nerves of the muscle tissue with burst signals to cause the muscle tissue to contract in synchrony with the heart. As a result, the heart is assisted in its contractions, thereby raising the stroke volume and thus cardiac output. Besides delivering therapeutic electrical pulses to the muscle, the pulse generator is quite often also coupled so as to also provide therapeutic electrical pulses to the heart. See, for example, U.S. Pat. No. 4,735,205 of Chachques et al., incorporated herein by reference.
Patients with chronic cardiac output deficiencies, although treatable through cardiomyoplasty, face an increased risk for cardiac arrhythmic episodes, such as ventricular tachycardia or fibrillation. These arrhythmic episodes may be life-threatening.
In order to treat these potentially life-threatening cardiac arrhythmias, some cardiac assist systems have been proposed which combine a muscle stimulator as well as a cardiac pacer-cardioverter-defibrillator. In such a manner a patient who has had a cardiomyoplasty may, in addition to receiving musclepowered cardiac assistance, also receive various types of therapeutic cardiac electrical stimulation. One example of such a system may be seen in the U.S. Pat. No. 5,251,621 issued to Collins and entitled "Arrhythmia Control Pacer Using Skeletal Muscle Cardiac Graft Stimulation. "
One problem associated with devices which combine a muscle stimulator as well as a cardiac pacer-cardioverter-defibrillator is that the muscle stimulation may interfere with the reliable sensing of cardiac events. During ventricular arrhythmias, such as ventricular fibrillation or ventricular tachycardia (hereafter "VF" and "VT" respectively) the cardiac signals may have very low amplitudes. This is especially the case during VF. The stimulation of the muscle wrap at that time could thus interfere with reliably sensing the VF or VT due to post-pace polarization, cross talk, et cetera.
The U.S. Pat. No. 5,251,621 issued to Collins offers one solution to this problem. The Collins patent discloses a cross channel blanking control signal to disable pacemaker sensing during generation of a skeletal muscle stimulation pulse. This is intended to prevent the pacemaker from incorrectly classifying a skeletal muscle stimulation pulse as an episode of intrinsic cardiac activity. At all times, however, muscle stimulation is continued. In fact, during arrhythmic events besides muscle stimulation continuing, Collins discloses adjusting various parameter of the muscle stimulation bursts, such as pulse amplitude, duration as well as the interval between pulses within a burst. One problem with this approach, however, is the continuation of skeletal muscle stimulation may interfere with the reliable sensing of the arrhythmia. Moreover, adjusting the various parameters of the muscle stimulation signal, such as amplitude or duration, creates an even greater likelihood that the device will not be able to reliably sense the arrhythmia.
Rapid detection of a cardiac tachyarrhythmia, and especially VF, is very important. A typical cardiac pacer-cardioverter-defibrillator detection algorithm requires the detection of a certain number of tachyarrhythmic events within a specified time period. In the case of VF detection, these devices will typically initiate the charging of a cardiac output circuit. This charging period may last between 1 to 21 seconds, depending on the therapy to be delivered. Following charging, the detection algorithm would once again confirm VF and deliver the therapy. Once the therapy was delivered, the detection algorithm would remain active until the tachyarrhythmic episode termination was confirmed.
At high energy levels, the period from tachyarrhythmia detection until tachyarrhythmia termination confirmation and muscle therapy reactivation could be extremely long, up to 35 seconds, or even longer. The consequence of this inhibition of the cardiac assistance during an episode of tachyarrhythmia is that cardiac output is highly compromised. In addition, while in fibrillation the threshold to achieve defibrillation through electrical shock rises exponentially. Higher defibrillation thresholds, however, mean the device must feature larger capacitors or higher voltages or both.